On Wed, 05 Dec 2001 17:56:36 +1030, et_al at my-deja.com wrote:
>On 2 Dec 2001 20:23:06 GMT, dag.stenberg at nospam.helsinki.fi wrote:
>>>2) increasing the permeability for Cl- will always cause inhibition, but
>>this can occur without any change in membrane potential (because of
>>"short-circuiting")
>>Um..no, not always. It depends on the concentration of Cl- in and
>outside the cell. For example in the rat superior suprachiasmatic
>nucleus (and probably also that of most mammals), GABA is excitatory
>during the day and inhibitory at night. The difference is that during
>the day the extracellular fluid has a low Cl- concentration so opening
>the GABA receptor causes Cl- to flow out of the cell, not into it.
>>See:
>>Wagner S, et al (1997)
>"GABA in the mammalian suprachiasmatic nucleus and it's role in diurnal
>rhythmicity"
>Nature vol 386; p173-7
>>Katz's "Beyond neurotransmission - Neuromodulation and it's importance
>for information processing" Oxford Univ Press, 1999 also goes into some
>detail about this on, from memory, pages 57-62.
>>About the best that can be said is that increasing membrane Cl-
>permeability will most often cause inhibition, but not always.
>>Ian
I have to get the original and go through it. I can't seem to reach
the Nature site right now and all I have is the abstract from PubMed.
Are these cells that function on the graded potential without action
potentials? Or does the Cl- change sufficiently to drive the reversal
potential above threshold? Or are the depolarizations summating with
other depolarizations sufficiently to reach threshold while at the
same time the synapse is distant enough so that the short-circuiting
effect is less significant? If I find out from the original paper,
I'll post it here.